Objective: We aimed to study the prevalence of visual memory dysfunction among epilepsy patients and identify the predictors that could contribute to the impairment.
Materials and Methods: This was a cross-sectional study. We analyzed 250 patients with epilepsy from neurology clinic at our tertiary center. Assessment of visual memory was done using Wechsler Memory Scale-IV (WMS-IV) with scores from subsets of visual reproduction I, II and designs I, II contributing to visual memory index (VMI) score. The correlation between continuous variables was analyzed using Pearson correlation; whereas the VMI scores of different factors were analyzed via a 1-way ANOVA test. The statistical significance was set at P < 0.05.
Results: The prevalence of visual memory dysfunction in our epilepsy population was 37.2%. Analysis of individual predictors showed that older patients, lower educational level, combined generalized and focal types of epilepsy, longer duration of epilepsy, greater number of antiepileptic drugs (AEDs) used, and abnormal neuroimaging contributed to poor visual memory. Multiple logistic regression analysis showed that educational level, types of epilepsy, and the number of AEDs used were significant predictors for visual memory impairment.
Conclusion: Visual memory dysfunction in patients with epilepsy was due to manifold confounding factors. Our findings enabled us to identify patients with visual memory dysfunction and modifiable factors that contribute to it. WMS-IV is a suitable assessment tool to determine visual memory function, which can help clinicians to optimize the patients' treatment.
MATERIALS AND METHODS: To examine this hypothesis, in the present study, the associations between CYP3A5 variants (rs776746 and rs1419745) and response to carbamazepine and valproic acid monotherapy in Malaysian epileptic patients were evaluated.
RESULTS: A total of 288 Malaysian epileptic patients were recruited and further reviewed, of whom 63 patients were on carbamazepine monotherapy, and 85 patients were on valproic acid monotherapy. There was no patient with drug hypersensitivity syndrome within the population. Subjects were genotyped by using Sequenom MassARRAY platform. This study found a significant association of CYP3A5 rs776746 with the carbamazepine treatment response in total patients (p = 0.026) and Malay ethnic subgroup (p = 0.006). In addition, a marginal significant association of CYP3A5 rs1419745 with carbamazepine treatment response was reported in the Malays. Similarly, CYP3A5 rs776746 was associated with valproic acid response in total patients (p = 0.037) and Malays (marginal p = 0.05).
CONCLUSION: Our findings suggest that CYP3A5 polymorphisms affect carbamazepine and valproic acid response in Malaysian epileptic patients.
SUMMARY: A 29-year-old woman undergoing contrast-enhanced computed tomography developed lesions over her trunk starting 6 hours after imaging. Although initially diagnosed as an allergy to the radiocontrast agent, the condition progressively worsened into toxic epidermal necrolysis-drug reaction with eosinophilia and systemic symptoms overlap syndrome, despite adequate hydration and treatment. Investigation of the patient's medications revealed that she had been switched from brand-name to generic levetiracetam a week before the onset of symptoms. Levetiracetam was immediately discontinued, with the patient recovering after 2 weeks of intensive care. Adverse drug reaction analysis identified excipients in generic levetiracetam as the likely cause of the severe reaction.
CONCLUSION: This is the first reported case of severe cutaneous drug allergy after a brand-to-generic switch for levetiracetam. Brand-to-generic switches of medications can potentially cause severe allergic reactions due to differences in excipients.
METHODS: DNA was extracted from eighty-six patients. The patients were genotyped by AS-PCR. Computational modeling of the HLA-B*15:02 followed by docking studies were performed to screen 26 AEDs that may induce ADR among HLA-B*15:02 carriers.
RESULTS: Odd ratio for CBZ induced SJS/TEN and HLA-B*15:02 was 609.0 (95% CI: 23-15873; p=0.0002). Molecular modeling studies showed that acetazolamide, ethosuxiamide, lamotrigine, oxcarbazepine, phenobarbital, phenytoin, primidone and sodium-valproate may induce ADR in HLA-B*15:02 carriers alike CBZ. Conclusion. We confirmed HLA-B*15:02 as a predictor of SJS/TEN and recommend pre-screening. Computational prediction of DIHR is useful in personalized medicine.